The contrasts between disbelief and belief showed increased signal in the anterior insula, a region involved in the sensation of taste, the perception of pain, and the feeling of disgust, indicating that “false propositions might actually disgust us,” the authors state. “Our results appear to make sense of the emotional tone of disbelief, placing it on a continuum with other modes of stimulus appraisal and rejection,” they add.
Uncertainty evoked a positive signal in the anterior cingulate cortex (ACC) and a decreased signal in the caudate, a region of the basal ganglia, which plays a role in motor action. Noting that both belief and disbelief showed an increased signal in the caudate compared to uncertainty, the authors suggest that the basal ganglia may play a role in mediating the cognitive and behavioral differences between decision and indecision.
The study raises the possibility that the differences between belief, disbelief and uncertainty may one day be reliably distinguished by neuroimaging techniques. They conclude: “This would have obvious implications for the detection of deception, for the control of the placebo effect during the process of drug design, and for the study of any higher-cognitive phenomenon in which the differences between belief, disbelief, and uncertainty might be a relevant variable.” (via.)
Everyone experiences social stress, whether it is nervousness over a job interview, difficulty meeting people at parties, or angst over giving a speech. In a new report, UCLA researchers have discovered that how your brain responds to social stressors can influence the body’s immune system in ways that may negatively affect health.
Lead author George Slavich, a postdoctoral fellow at the UCLA Cousins Center for Psychoneuroimmunology, and senior author Shelley Taylor, a UCLA professor of psychology, show that individuals who exhibit greater neural sensitivity to social rejection also exhibit greater increases in inflammatory activity to social stress. [...]
The researchers recruited 124 individuals — 54 men and 70 women — and put them into two awkward social situations. First, in the lab, the volunteers completed the Trier Social Stress Test (TSST), which involves preparing and delivering an impromptu speech and performing difficult mental arithmetic, both in front of a socially rejecting panel of raters wearing white lab coats. Mouth swabs were taken before and after the public-speaking tasks to test for changes in two key biomarkers of inflammatory activity — a receptor for tumor necrosis factor-? (sTNF?RII) and interleukin-6 (IL-6).
In a second session, 31 of the participants received an MRI brain scan while playing a computerized game of catch with what they believed were two other real people. The researchers focused on two areas of the brain known to respond to social stress — the dorsal anterior cingulate cortex (dACC) and the anterior insula.
At first, the game was between all three “players.” Halfway through the game, however, the research subject was excluded, leading to an experience of social rejection. The researchers then examined how differences in neural activity during social rejection correlated with differences in inflammatory responses to the TSST.
Their results showed that individuals who exhibited greater neural activity in the dorsal anterior cingulate cortex and anterior insula during social rejection in the brain scanner also exhibited greater increases in inflammatory activity when exposed to acute social stress in the lab.
“This is further evidence of how closely our mind and body are connected,” Slavich said. “We have known for a long time that social stress can ‘get under the skin’ to increase risk for disease, but it’s been unclear exactly how these effects occur. To our knowledge, this study is the first to identify the neurocognitive pathways that might be involved in inflammatory responses to acute social stress.” [...]
One critical question raised by the present findings is why neural sensitivity to social rejection would cause an increase in inflammation. There are several possible reasons, the authors note. For one, since physical threats have historically gone hand in hand with social threat or rejection, inflammation may be triggered in anticipation of a physical injury. Inflammatory cytokines — proteins that regulate the immune system — are released in response to impending (or actual) physical assault because they accelerate wound-healing and reduce the risk of infection.
This may also be of interest: Tylenol (acetaminophen) eases social anxiety.
The scientists, including collaborators at the University of Colorado at Boulder and the University of Maryland, studied 20 adolescent boys. On average they had been on probation 139 of the last 180 days; 19 of the 20 had the psychiatric diagnosis of conduct disorder, and all had diagnoses of substance use disorder. They had been abstinent, however, an average of about five weeks when studied. They were compared with 20 other boys who did not have serious antisocial or drug problems, but who were of similar age, ethnicity, and home neighborhoods.
All played a computerized risk-taking game that repeatedly presented a choice between a cautious and a risky behavior: press the left button and always win one cent, or press the right button and either win five cents or lose ten cents. The scientists examined brain activation with functional magnetic resonance imaging (fMRI) as the boys decided to press right or left, and then as they experienced wins or losses after right presses.
Brain activation differed dramatically in the two groups. The anterior cingulate cortex monitors changing rewards and punishments, and then sends that information to another brain region (dorsolateral prefrontal cortex), which regulates one’s choices among possible behaviors. During decision-making, antisocial boys had significantly less brain activity than normals in both of those regions, and also in other decision-making areas (orbitofrontal cortex, amygdala, insula).
This just in, from the turbo-weird category:
Could acetaminophen (tylenol) ease social pain? – “[They] investigated this connection through two experiments. In the first experiment, 62 volunteers took [1 gram] daily of either acetaminophen or a placebo. Each evening, participants reported how much they experienced social pain using a ‘Hurt Feelings Scale’ — a measurement widely accepted by psychologists as a valid measure of social pain. Hurt feelings and social pain decreased over time in those taking acetaminophen, while no change was observed in the placebo group. [...] In the second experiment, 25 healthy volunteers took [2 grams] daily of either [tylenol] or a placebo. After three weeks of taking the pills, subjects participated in a computer game rigged to create feelings of social rejection. fMRI [brain scans] employed during the game revealed that acetaminophen reduced neural responses to social rejection in brain regions associated with the distress of social pain and the affective component of physical pain (the dorsal anterior cingulate cortex and anterior insula).”